Evidence map›Paper›PMID 25921341›Full record

Trial reportMucosal immunology2016

Modulation of nasopharyngeal innate defenses by viral coinfection predisposes individuals to experimental pneumococcal carriage.

S Glennie, J F Gritzfeld, S H Pennington, M Garner-Jones, N Coombes, M J Hopkins, C F Vadesilho, E N Miyaji, D Wang, A D Wright and 3 more

Open access · hybridAbstract readClinical Trial
In one paragraph

Trial report in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.0field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 49 citations in OpenAlex.

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  15. Diverse Mechanisms of Protective Anti-Pneumococcal Antibodies.Frontiers in cellular and infection microbiology · 2022
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 2 countries.

S GlennieRespiratory Infection Group, Liverpool School of Tropical Medicine, Liverpool, UK.
J F GritzfeldRespiratory Infection Group, Liverpool School of Tropical Medicine, Liverpool, UK.
S H PenningtonRespiratory Infection Group, Liverpool School of Tropical Medicine, Liverpool, UK.
M Garner-JonesRespiratory Infection Group, Liverpool School of Tropical Medicine, Liverpool, UK.
N CoombesRespiratory Infection Group, Liverpool School of Tropical Medicine, Liverpool, UK.
M J HopkinsLiverpool Specialist Virology Centre, Royal Liverpool and Broadgreen University Hospital, Liverpool, UK.
C F VadesilhoCentro de Biotecnologia, Instituto Butantan, Sao Paulo, Brazil.
E N MiyajiCentro de Biotecnologia, Instituto Butantan, Sao Paulo, Brazil.
D WangTropical Clinical Trial Unit, Liverpool School of Tropical Medicine, Liverpool, UK.
A D WrightRespiratory Infection Group, Liverpool School of Tropical Medicine, Liverpool, UK.
A M CollinsRespiratory Infection Group, Liverpool School of Tropical Medicine, Liverpool, UK.
S B GordonRespiratory Infection Group, Liverpool School of Tropical Medicine, Liverpool, UK.
D M FerreiraRespiratory Infection Group, Liverpool School of Tropical Medicine, Liverpool, UK.
Liverpool School of Tropical Medicine · GBInstituto Butantan · BRRoyal Liverpool and Broadgreen University Hospital NHS Trust · GB

Funding

Medical Research Council MR/K01188X/1Medical Research Council MR/M011569/1
6 · The paper itself

Abstract

Increased nasopharyngeal colonization density has been associated with pneumonia. We used experimental human pneumococcal carriage to investigate whether upper respiratory tract viral infection predisposes individuals to carriage. A total of 101 healthy subjects were screened for respiratory virus before pneumococcal intranasal challenge. Virus was associated with increased odds of colonization (75% virus positive became colonized vs. 46% virus-negative subjects; P=0.02). Nasal Factor H (FH) levels were increased in virus-positive subjects and were associated with increased colonization density. Using an in vitro epithelial model we explored the impact of increased mucosal FH in the context of coinfection. Epithelial inflammation and FH binding resulted in increased pneumococcal adherence to the epithelium. Binding was partially blocked by antibodies targeting the FH-binding protein Pneumococcal surface protein C (PspC). PspC epitope mapping revealed individuals lacked antibodies against the FH binding region. We propose that FH binding to PspC in vivo masks this binding site, enabling FH to facilitate pneumococcal/epithelial attachment during viral infection despite the presence of anti-PspC antibodies. We propose that a PspC-based vaccine lacking binding to FH could reduce pneumococcal colonization, and may have enhanced protection in those with underlying viral infection.

Indexed as

Immunity, InnateAdolescentAdultAmino Acid SequenceAntibodies, BacterialBacterial AdhesionBacterial ProteinsBinding SitesCoinfectionComplement Factor HEpitope MappingFemaleGene Expression RegulationHumansImmunity, MucosalMaleAntibodies, BacterialBacterial ProteinsComplement Factor HSpsA protein, Streptococcus pneumoniae

Identifiers

PMID25921341
PMCPMC4703943
OpenAlexW2010149386

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.